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Mini Review: Structure and Function of Nematode Phosphorylcholine-Containing Glycoconjugates

Buitrago, Geraldine, Duncombe-Moore, Josephine, Harnett, Margaret M., Harnett, William·2021·Frontiers in Tropical Diseases
DOI 10.3389/fitd.2021.769000
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Abstract

An unusual aspect of the biology of nematodes is the covalent attachment of phosphorylcholine (PC) to carbohydrate in glycoconjugates. Investigation of the structure of these molecules by ever-increasingly sophisticated analytical procedures has revealed that PC is generally in phosphodiester linkage with C6 of N-acetylglucosamine (GlcNAc) in both N-type glycans and glycosphingolipids. Up to five PC groups have been detected in the former, being located on both antenna and core GlcNAc. The PC donor for transfer to carbohydrate appears to be phosphatidylcholine but the enzyme responsible for transfer remains to be identified. Work primarily involving the PC-containing Acanthocheilonema viteae secreted product ES-62, has shown that the PC attached to nematode N-glycans possesses a range of immunomodulatory properties, subverting for example, pro-inflammatory signalling in various immune system cell-types including lymphocytes, mast cells, dendritic cells and macrophages. This has led to the generation of PC-based ES-62 small molecule analogues (SMAs), which mirror the parent molecule in preventing the initiation or progression of disease in mouse models of a number of human conditions associated with aberrant inflammatory responses. These include rheumatoid arthritis, systemic lupus erythematosus and lung and skin allergy such that the SMAs are considered to have widespread therapeutic potential.

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FIGURE 3 ES-62/phosphorylcholine (PC) desensitises immune system cell signalling in vitro . (A) The B cell antigen receptor (BCR) signals via ITAM-containing Ig a / b accessory molecules to recruit proliferative signalling pathways like the ERK MAPK cascade in a tyrosine kinase-dependent manner. PC/ES-62 desensitises the BCR both by recruiting SHP-1 to dephosphorylate Ig b and uncouple downstream signalling and by inducing DUSP2 dephosphorylation of the TEY activation motif of ERK1/2. (B) Fc ϵ RI-mediated degranulation requires calcium and PKC a signalling whilst, at least in some mast cell subsets, cytokine secretion also requires crosstalk with MyD88 signalling and all of these elements are targeted by PC/ES-62. (C) TLR4 homodimer and TLR1/2 heterodimer located at the cell surface on dendritic cells and macrophages signal through the adaptor proteins TIRAP and MyD88 in response to LPS and bacterial lipopeptide (e.g., PAM3CSK4) respectively. TLR9, which responds to unmethylated cytosine-phosphate-guanine (CpG) DNA, also signals through MyD88. MyD88 stimulates NFk B regulated proin fl ammatory cytokine production. ES-62 and PC-conjugated proteins subvert TLR4-MyD88 signalling to reduce proin fl ammatory cytokine secretion in response to TLR1/2, TLR4 and TLR9 ligation. Small molecule analogues 11a and 12b interact directly with MyD88 thereby similarly inhibiting cytokine production. TLR3 signalling, which is MyD88independent, is not affected by these anti-in fl ammatory agents. ES-62 is internalised by macrophages and may also directly interact with MyD88 via its PC moieties.
FIGURE 3 ES-62/phosphorylcholine (PC) desensitises immune system cell signalling in vitro . (A) The B cell antigen receptor (BCR) signals via ITAM-containing Ig a / b accessory molecules to recruit proliferative signalling pathways like the ERK MAPK cascade in a tyrosine kinase-dependent manner. PC/ES-62 desensitises the BCR both by recruiting SHP-1 to dephosphorylate Ig b and uncouple downstream signalling and by inducing DUSP2 dephosphorylation of the TEY activation motif of ERK1/2. (B) Fc ϵ RI-mediated degranulation requires calcium and PKC a signalling whilst, at least in some mast cell subsets, cytokine secretion also requires crosstalk with MyD88 signalling and all of these elements are targeted by PC/ES-62. (C) TLR4 homodimer and TLR1/2 heterodimer located at the cell surface on dendritic cells and macrophages signal through the adaptor proteins TIRAP and MyD88 in response to LPS and bacterial lipopeptide (e.g., PAM3CSK4) respectively. TLR9, which responds to unmethylated cytosine-phosphate-guanine (CpG) DNA, also signals through MyD88. MyD88 stimulates NFk B regulated proin fl ammatory cytokine production. ES-62 and PC-conjugated proteins subvert TLR4-MyD88 signalling to reduce proin fl ammatory cytokine secretion in response to TLR1/2, TLR4 and TLR9 ligation. Small molecule analogues 11a and 12b interact directly with MyD88 thereby similarly inhibiting cytokine production. TLR3 signalling, which is MyD88independent, is not affected by these anti-in fl ammatory agents. ES-62 is internalised by macrophages and may also directly interact with MyD88 via its PC moieties.CC-BY · From the PDF
FIGURE 4 ES-62/PC-mechanism of action in collagen-induced arthritis and ovalbumin-induced airway hyperresponsiveness. In collagen induced arthritis (CIA), during the initiation phase, gd T cells and T helper (Th)17 cells secrete interleukin (IL)-17 and IL-22 causing joint pathology. By contrast, during established disease IL22 acts to limit pathology, indicating that this cytokine plays dual pathogenic and protective roles in CIA. Treatment with ES-62 or small molecule analogue (SMA) 11a inhibits IL-17 production and ES-62 promotes protective IL-22 production as well as restoring regulatory B cell (Breg) responses to counter pathogenic effector B cell (Beff) responses including collagen-speci fi c IgG2a production, thereby substantially reducing arthritis. In ovalbumin-induced airway hyperresponsiveness (AHR), in fl ammatory immune system cells such as eosinophils and neutrophils in fi ltrate the lungs, generating IL-4 production, and a Th2 anti-in fl ammatory immunological phenotype is evident in immune cells in draining lymph nodes as the cells secrete IL-5 and IL-13 upon re-stimulation ex vivo . ES-62 and SMA administration reduce the in fi ltration of in fl ammatory immune cells and the former has also been shown to inhibit the ex vivo production of IL-5 and IL-13. Moreover, ES-62-activity in this model has been found to be dependent on IFNg and in addition, similar to CIA, the helminth product increases IL-10-producing Bregs.
FIGURE 4 ES-62/PC-mechanism of action in collagen-induced arthritis and ovalbumin-induced airway hyperresponsiveness. In collagen induced arthritis (CIA), during the initiation phase, gd T cells and T helper (Th)17 cells secrete interleukin (IL)-17 and IL-22 causing joint pathology. By contrast, during established disease IL22 acts to limit pathology, indicating that this cytokine plays dual pathogenic and protective roles in CIA. Treatment with ES-62 or small molecule analogue (SMA) 11a inhibits IL-17 production and ES-62 promotes protective IL-22 production as well as restoring regulatory B cell (Breg) responses to counter pathogenic effector B cell (Beff) responses including collagen-speci fi c IgG2a production, thereby substantially reducing arthritis. In ovalbumin-induced airway hyperresponsiveness (AHR), in fl ammatory immune system cells such as eosinophils and neutrophils in fi ltrate the lungs, generating IL-4 production, and a Th2 anti-in fl ammatory immunological phenotype is evident in immune cells in draining lymph nodes as the cells secrete IL-5 and IL-13 upon re-stimulation ex vivo . ES-62 and SMA administration reduce the in fi ltration of in fl ammatory immune cells and the former has also been shown to inhibit the ex vivo production of IL-5 and IL-13. Moreover, ES-62-activity in this model has been found to be dependent on IFNg and in addition, similar to CIA, the helminth product increases IL-10-producing Bregs.CC-BY · From the PDF

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Metadata

Authors
Buitrago, G., Duncombe-Moore, J., Harnett, M. M., & Harnett, W.
Venue
Frontiers in Tropical Diseases
Publisher
Frontiers Media SA
Published
2021-12-14
Volume
2
ISSN
2673-7515
DOI
10.3389/fitd.2021.769000
Cited by
8
References
3
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Biotechnology and Biological Sciences Research Council

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